Anesthesia & renal physiology- week 4 Flashcards
Normal ECF H+ is:
40nEq/L
Acid-base physiology is all about
H+ ion concentrations
a low pH corresponds to a:
high H+ concentration
Whats the normal pH or arterial blood?
7.4
what is the normal pH or venous blood and interstitial fluids
7.35
bc of the extra amounts of carbon dioxide released from the tissues for Carbonic acid (H2CO3)
acid is defined as a proton (H+)
donor
base is defined as a proton (H+)
acceptor
a weak acid or base reversibly
donates or accepts protons
What is the henderson-hasselbalch equation?
describes the relationship btwn pH, paco2, and bicarb
what is the solubility coefficient for Co2?
0.03 mmol/mmhg at body temperature
this means that 0.03 millimole of H2Co3 (carbonic acid is present in the blood for each mmHg Pco2 measurement
the HCO3- concentration is regulated mainly by:
the kidneys
The PCO2 in extracellular fluid is controlled by:
rate of respiration
WHen are buffers most efficient?
when pH= pKa
Solutions of ____ ____ or _____ act as ______ as they minimize pH changes by donating or accepting electrons
weak acids or bases act as buffers
What are the body buffers?
Bicarbonate (H2CO3/HCO3)
Hemoglobin
Intracellular proteins
Phosphate
Ammonia
buffer systems do not ______ or ______ ______ but only keep them tied up until balance can be restored
Buffer systems do not eliminate or Add H+
what are the 3 primary systems that regulate the H+ concentration in the body fluids to prevent acidosis or alkalosis?
1.) the chemical acid-base buffer systems of the body fluids (immediately combine w an acid or base to prevent excessive changes in H+ concentration)
2.) Respiratory center
3.) Kidneys - by far the most powerful acid-base regulatory system
what is the bicarbonate buffer system?
hydration of co2 is catalyzed by carbonic anhydrase
-pKa of bicarb is 6.1 (far from plasma pH)
-most powerful extracellular buffer in the body
What is the renal compensation during acidosis?
increased HCO3- reabsorption
-co2 combines w water to form carbonic anhydrase (H2CO3) which rapidly dissociated into H+ and HCO3-
-H+ is SECRETED into the proximal tubule and bicarb is reabsorbed into the blood
Where is H+ secreted into the tubular fluid by the sodium-hydrogen counter-transport?
PCT
TAL
DCT
80-90% of filtered bicarb is reabsorbed in the:
proximal tubule
10-20% of bicarb reabsorbed in the:
distal tubule
in the distal tubule a _____ ____ exists which can establish a steep gradient for acidifying urine
H+ pump
What is the phosphate buffer?
effective buffer in the tubular fluid
pKa of 6.8
- important buffering intracellular fluid bc the concentration of phosphate in this fluid is many times the extracellular fluid.
the intracellular fluid is lower than that of the extracellular fluids and therefor is usually closer to the pKa of the phosphate buffer system compared w extracellular fluid
What is the ammonium (NH4) buffer system?
important tubular fluid buffer
-PCT
-TAL
-DCT
ammonium synthesized from glutamine (from amino acids in liver)
bicarb generated in the synthesis process
- collecting tubules: production of NH4
- more important that phosphar buffer system
-composed of ammonia (NH3) and ammoniumion (NH4)
In chronic acidosis- what is the dominant mechanism by which acid is eliminated?
NH4+ excretion (Ammoniumion)
Left =
proximal tubules using glutamine
right=
collecting tubules using H+
an increase in extracellular H+ concentration stimulates:
renal glutamine metabolism = increased formation of NH4+ and new HCO3- to be used in H+ buffering
contraction alkalosis can occur with?
long term diuretic use
in alkalosis there is a:
negative net acid secretion
What is base excess?
The amount of acid or base that must be added to return blood pH to 7.4 w paco2 of 40mmHg and temp 37
what does a positive base excess mean?
metabolic alkalosis
what does a negative base excess mean?
metabolic acidosis
the most important stimuli for increasing H+ secretion during acidosis are:
1.) An increase in PCO2 of the extracellular fluid in resp. acidosis
2.) an increase in H+ concentration of the extracellular fluid
What causes metabolic alkalosis?
vomiting
diuretics
hypokalemia
hypochloremia
hypovolemia
hypocalcemia
ventricular arrhythmias
dig toxicity
hypoventilation
curve shifts to left
decreased CO
factors the maintain metabolic alkalosis:
-decreased GFR
-Volume contraction
-hypokalemia
-hypochloremia
-passive backflux of HCO3-
-aldosterone
Metabolic alkalosis: Paco2 increases
PaCO2 increases 0.5-0.6 for 1 meq increase in hco3-
metabolic alkalosis: the last 2 digits of the pH should approximate HCO3- + ?
15
metabolic acidosis: paco2- hco3-
PaCO2– [HCO3−] × 1.5 + 8
metabolic acidosis: paco2 decreases _____ per 1 mEq/L hco3
1.2
metabolic acidosis: the last 2 digits of pH:
The last two digits of the pH – [HCO3−] + 15
treatment for metabolic alkalosis:
-intravascular volume expansion
-potassium
-0.9% NS
What causes elevated anion gap?
-Uremia
-Ketoacidosis
-lactic acidosis
-menthanol
-ethylene glycol
-salicylates
-paraldehyde
whats an anion gap?
helps us determine the cause of acidosis
what is a normal anion gap?
8-12 mEq/L
Major cations - major anions
Na - Cl + HCO3
Anion gap acidosis
pH < 7.35
anion gap >14 (13)
Accumulation of acid= gap acidosis
Mnemonic: MUDPILES
-methanol
-uremia
-diabetic ketoacidosis
-paraldehyde
-isoniazid
-lactate
-ethanol
-salicylates
Non-gap acidosis
pH <7.35
anion gap <14
Loss of bicarb or ECF dilution
Mnemonic: HARDUP
-hypoaldosteronism
-acetazolamide
-renal tubular acidosis
-diarrhea
-uterosigmoid fistula
-pancreatic fistula
HCL administration
Saline administration
how does the body compensate for metabolic acidosis
PaCO2 decreases by 1-1.5 mmHg for every HCO3- decrease of 1 mEq/L
How do you treat metabolic acidosis?
Lactic acidosis: IVF, o2, cardiopulmonary support
diabetic ketoacidosis: IVF, insulin
Uremia or drug-induced: dialysis
How does the body compensate for metabolic alkalosis?
the body will retain CO2 by reducing minute ventilation
paco2 increases by 0.5-1 mmHg for every HCO3- an increase of 1 mEq/L
How do you treat metabolic alkalosis?
Acetazolamide (carbonic anhydrase inhibitor) increases renal excretion of HCO3-
spirnolactone- (mineralcorticoid antagonist)
dialysis
NaHCO3– do not give to pt w resp failure (co2 will go up)
What are the physiologic effects of acidosis?
-potassium increases 0.6 mEq/L for each 0.1 unit decrease in pH
-a rightward shift of the oxy-hemoglobin dissociation curve
-decreased cardiac contractility
-decreased responsiveness to catecholamines
Balanced salt solutions:
increase pH and HCo3-
by metabolism of lactate to bicarb
0.9% saline:
tends to decrease pH and HCO3-
Halving minute ventilation:
doubles Paco2 and doubles cerebral blood flow
Respiratory alkalosis may produce:
-hypokalemia
-hypocalcemia
-cardiac dysrhythmias
-bronchoconstriction
-HoTN
-dig toxicity
compensation in acute resp acidosis:
acute: expect a 1 meQ/L increase in bicarb for every 10 mmhg increase in CO2 (usually from 40 mmhg)
compensation in chronic resp acidosis:
chronic: expect a 4 mEq/L increase bicarb for every 10mmhg increase in co2
compensation in metabolic acidosis
co2 decreased 1.2 x the decrease in bicarb (usually from 24mEq)
compensation for respiratory alkalosis- acute
Acute: expect 2 mEq/L decrease in HCO3- for every 10 mmHg decrease in CO2
compensation for chronic respiratory alkalosis:
expect 4 mEq/L decrease in bicarb for every 10 mmHg in co2
compensation for metabolic alkalosis; ;
co2 increases by 0.7 x the increase in HCO3
